药物难治性癫痫的手术治疗效果

目的探讨药物难治性癫痫的外科治疗的手术要点和效果。方法回顾性分析药物难治性癫痫患者26例资料。依据术前临床表现、影像学、脑电图等资料制定个性化手术方案,术后服用丙戊酸钠片;按Engel′s标准评判癫痫发作控制情况来评定手术效果。结果术后随访3-24个月结果:Engel′sⅠ级15例(57.7%),Ⅱ级7例(26.9%),Ⅲ级3例(11.5%),Ⅳ级1例(3.8%),总有效率达84.6%。结论制定个性化手术方案可以使药物难治性癫痫获得满意疗效。     

难治性癫痫的药物治疗进展

报告氟佳嗪、莨菪类药、丙戊酸钠、利多卡因、青阳参对难治性癫痫的治疗。     

难治性癫痫经药物治疗的护理观察

目的分析探讨护理对经药物治疗的难治性癫痫患者的临床效果。方法选取2004年3月至2011年3月期间,在我院进行药物治疗的难治性癫痫患者164例,随机将患者分为对照组和观察组,对照组患者采取常规护理,观察组患者采取干预护理,分别分析两组患者临床治疗效果,月平均发作次数以及并发症的发生情况。结果和对照组相比,观察组患者治疗有效率明显升高,月平均发作次数明显减少,发生恶心、斑丘疹、食欲不振和视力模糊等并发症的发生率明显降低,差异具有统计学意义（P〈0.05）。结论干预护理可以有效增加经药物治疗的难治性癫痫患者的临床有效率,对提高临床质量有积极的促进作用,值得临床广泛推广。     

难治性癫痫治疗方法探讨

癫痫(epilepsy,EP)在临床上是一种常见病,是多种原因引起的慢性脑功能紊乱所致的综合征。EP是脑内病灶部位的神经细胞异常放电引起的运动、感觉、意识、行为和自主神经的不同障碍,具有反复发作,亦可自然缓解为特征的一组疾病。     

难治性癫痫治疗方法探讨

癫痫(epilepsy,EP)在临床上是一种常见病,是多种原因引起的慢性脑功能紊乱所致的综合征.EP是脑内病灶部位的神经细胞异常放电引起的运动、感觉、意识、行为和自主神经的不同障碍,具有反复发作,亦可自然缓解为特征的一组疾病.一般说癫痫患者通过正规治疗,80%患者可以控制或缓解,但有20%左右患者使用一种或多种抗癫痫药物,未能控制,仍有反复发作,称为难治性EP或耐药性EP[1].     

儿童难治性癫痫的治疗进展

癫痫为临床常见儿童神经系统疾病,相较于成人癫痫患者,儿童癫痫病因与临床治疗手段、临床表现上有明显差异。癫痫发作与抗癫痫药物的大量应用,对患儿学习、生活与成长发育均造成严重困扰。传统抗癫痫药物会产生较为严重的不良反应,且难以完全治愈,患儿难以耐受。近年来,随着医疗不断发展,抗癫痫治疗也得到极大的进展,特别是对儿童难治性癫痫,其治疗手段已经获得极大突破。目前,针对儿童难治性癫痫,治疗方法较多,本文对儿童难治性癫痫的治疗进展作分析,现综述如下。     

西比灵辅治小儿难治性癫痫

自1994年以来，应用西比灵辅治小儿难治性癫痫32例，采用自身对照法对患儿进行了临床观察，现将结果报告如下：     

丙缬草酰胺片治疗28例难治性癫痫疗效观察

自 198 7年 8月以来 ,用丙缬草酰胺片 (癫健安 )治疗 2 8例难治性癫 ,取得较满意的疗效 ,现报道如下。资料和方法　全部病例为 1987年 9月～ 1999年 3月 ,因大发作到急诊科抢救病例共 2 8例 ,均为强直—阵挛性发作 ,其中 3例为癫持续状态 ,在急诊科大剂量镇静剂方可控制发作。全部病例经过脑电图及病史确诊。按病因分类 ,先天性 (遗传性 )者 5例 ;外伤性 (颅脑外伤、挫伤、出血和缺血 )者 13例 ;感染性 (脑炎、脑膜炎后遗症 )者8例 ;颅内肿瘤 1例 ;不明原因于夜间睡眠中周期性 (每月一次 )大发作者 1例。男性 19例 ,女性 9例 ,年龄 15～…     

儿童难治性癫痫临床治疗的研究进展

癫痫发病人群中儿童是成年人发病的15倍,并且部分儿童患经治疗后仍出现反复发作的现象,逐渐发展为难治性癫痫,对患儿未来成长造成严重的影响。我国对于难治性癫痫治疗持续进行创新,但仍有部分患儿现行药物疗效不佳,本文就当前儿童难治性癫痫临床治疗进行总结。     

Anticonvulsant drugs for generalized tonic-clonic epilepsy

Introduction: Primary generalized tonic clonic seizures (pGTCS) are still linked to major concerns for the clinic and hazards for patients suffering from idiopathic generalized epilepsy (IGE), so a quick search of the most effective and appropriate therapy is needed to control them. The key criteria for proper treatment are syndromic diagnosis and distinction between newly diagnosed and refractory patients. Other criteria include age, gender and comorbidities.

Areas covered: Treatment for pGTCS has expanded in the last two years, with new antiepileptic drugs like perampanel joining valproic acid, lamotrigine, levetiracetam, topiramate, while further evidence-based data are required for zonisamide and lacosamide.

Expert opinion: Currently, valproic acid can be considered as a first choice in male or menopausal women, and in the absence of weight issue, both in adults and in children, and in the absence of side effects such as insomnia and headache. Today, valproic acid is not recommended in child-bearing age and in relation to possible cognitive problems, especially in children. Lamotrigine and levetiracetam can be a viable alternative as a first choice. Topiramate is also effective as a first choice, but concerns may arise from its potential cognitive and memory adverse side effects. Additionally, perampanel and lacosamide are promising treatments.     

托吡酯加用传统抗癫痫药治疗难治性癫痫部分性发作16例

目的：观察托吡酯加用传统抗癫痫药对难治性癫痫部分发作治疗的临床疗效和耐受性。方法：对16例难治性部分性发作患者加用托吡酯进行治疗,25mg/d为起始剂量,每周增加25mg,至200mg/d维持治疗,观察加用治疗前后癫痫发作频率的改变和耐受性。结果：观察24周后7例（43．8％）发作频率减少≥50％,其中3例（18．8％）停止发作,2例（12．5％）发作频率减少26％－49％,5例发作频率减少≤25％,1例发作频率明显增加,1例观察12周后失访。结论：托吡酯作为具有多重作用机制的抗癫痫新药,加用治疗难治性癫痫部分性发作的总有效率为56．3％（9／16）,无明显的必须停药的不良反应,耐受性良好。     

Pharmacotherapy of focal epilepsy

Introduction: Epilepsy is the most common neurological condition worldwide with significant psychosocial and physical morbidity. Its management requires expertise and good pharmacological knowledge of the available options.

Areas covered: This review covers the management of focal epilepsy addressing the common questions arising through the patients’ journey, including timing of starting initial treatment, monotherapy options, add-on treatment for refractory cases and withdrawal of medication during remission.

Expert opinion: Initiating anti-epileptic drug (AED) treatment requires assessment of patient preferences and of evidence of benefit and harm. Evidence of benefit will come primarily from randomised controlled trials, although in epilepsy, most trials are undertaken to inform regulatory decision and have important limitations for informing clinical decisions. Evidence about harm may come not only from randomised trials but also from other sources. Most patients will start treatment following a second focal seizure. Carbamazepine and lamotrigine are good initial monotherapy options. Newer AEDs have proof of efficacy as monotherapy but evidence is insufficient to recommend them as first-line treatments. For refractory cases, there are an increasing number of AEDs available, but evidence of efficacy is primarily from placebo-controlled trials, and there is no robust evidence to inform a choice among treatments.     

Eslicarbazepine acetate: a new option for the treatment of focal epilepsy

Background: Epilepsy is a neurological condition with an increased probability of seizure occurrence through time. Although many anti-epileptic drugs (AEDs) exist, they fail to treat seizures in 30% of patients with epilepsy. For these patients, new AEDs potentially more efficacious and safe are developed. Objective: To evaluate the effectiveness of eslicarbazepine acetate (ESL) in the treatment of patients with refractory epilepsy. Methods: A review of the literature was carried out using PubMed central. A direct contact with the drug manufacturer and developer was made. Results/conclusion: ESL is an AED that acts by inhibiting voltage-gated sodium channels. It has proved efficacious in the treatment of patients with refractory focal-onset epilepsy with a good safety profile. Evaluation of its use for treating other epileptic syndromes and its role as an initial treatment option for patients with epilepsy is warranted.     

多处软脑膜下横纤维切断治疗难治性癫痫30例

目的 解决难治性癫痫特别是位于重要功能区痫灶的手术处理。方法 对30例难治灶癫痫病人进行了病灶切除上皮层多处软脑膜下横纤维切断术,利用皮层电极反复描记,在手术显微镜下操作,直至整个术野棘尖波消失,脑电波全部趋于正常,术前术后均行神经心理学评定。结果术后随访2～27个月,显效率83．3—,有效率93．3%,随访期未见任何运动、感觉,语言功能的损害。结论 该手术疗效肯定,尤其在功能区手术,术后未出现手术并发症,取得了较好的癫痫发作控制及功能保护疗效。     

卡马西平、丙戊酸、拉莫三嗪、奥卡西平、托吡酯治疗初发癫痫患者的长期保留率对比

目的探讨卡马西平(CBZ)、丙戊酸(VPA)、拉莫三嗪(LTG)、奥卡西平(OXC)、托吡酯(TPM)治疗初发癫痫患者的长期保留率的差异。方法选取846例于2005年11月至2016年3月入我院的新诊断癫痫患者,依据患者意愿,分别选用卡马西平、丙戊酸、拉莫三嗪、奥卡西平、托吡酯单药治疗,将所有患者分为CBZ组、VPA组、LTG组、OXC组、TPM组5组,并通过随访2年,记录所有患者的药物长期保留率、不良反应、临床疗效、停药时间和停药原因。结果 846例患者中,共有643例(76.00%)2年内一直保持单药治疗,其中,CBZ组、VPA组、LTG组、OXC组、TPM组的保留率分别为73.42%(174/237)、74.48%(251/337)、85.56%(77/90)、78.13%(50/64)、77.12%(91/118),CBZ组和VPA组保留率与LTG组相比,差异有统计学意义(P<0.05),其他组间相比,差异无统计学意义(P>0.05);五组患儿的抗癫痫药物长期保留率组间比较,差异有统计学意义(P<0.05);五组成年患者的抗癫痫药物长期保留率组间比较,差异无统计学意义(P>0.05)。五组患者2年后临床疗效对比,差异无统计学意义(P>0.05)。依从性差是患者停止服药的首要原因。结论在5种药物中,LTG治疗初发癫痫患者的长期保留率最高,不同药物的临床疗效并无显著差异,导致患者停药的首要原因是依从性差。     

Clinical reappraisal of the influence of drug-transporter polymorphisms in epilepsy

Introduction: Although novel antiepileptic drugs (AEDs) have been recently released, the issue of drug resistance in epileptic patients remains unsolved and largely unpredictable.

Areas covered: We aim to assess the clinical impact of genetic variations that may influence the efficacy of medical treatment in epilepsy patients. Indeed, many genes, including genes encoding drug transporters (ABCB1), drug targets (SCN1A), drug-metabolizing enzymes (CYP2C9, CYP2C19), and human leucocyte antigen (HLA) proteins, may regulate the mechanisms of drug resistance in epilepsy. This review specifically focuses on the ABC genes, which encode multidrug resistance-associated proteins (MRPs) and may reduce the blood–brain barrier penetration of anticonvulsant AEDs.

Expert opinion: Drug resistance remains a crucial problem in epilepsy patients. Pharmacogenomic studies may improve our understanding of drug responses and drug resistance by exploring the impact of gene variants and predicting drug responses and tolerability.     

儿童难治性癫多药治疗及药物相互作用的研究进展

将相关文献进行归纳和整理,探讨新型抗癫药物拉莫三嗪、托吡酯、奥卡西平及左乙拉西坦在儿童难治性癫的多药治疗中药物间的相互作用、用法、用量和副作用。     

Antiarrhythmic drugs and epilepsy

For a long time it has been suspected that epilepsy and cardiac arrhythmia may have common molecular background. Furthermore, seizures can affect function of the central autonomic control centers leading to short- and long-term alterations of cardiac rhythm. Sudden unexpected death in epilepsy (SUDEP) has most likely a cardiac mechanism. Common elements of pathogenesis create a basis for the assumption that antiarrhythmic drugs (AADs) may affect seizure phenomena and interact with antiepileptic drugs (AEDs).Numerous studies have demonstrated anticonvulsant effects of AADs. Among class I AADs (sodium channel blockers), phenytoin is an established antiepileptic drug. Propafenone exerted low anti-electroshock activity in rats. Lidocaine and mexiletine showed the anticonvulsant activity not only in animal models, but also in patients with partial seizures. Among beta-blockers (class II AADs), propranolol was anticonvulsant in models for generalized tonic-clonic and complex partial seizures, but not for myoclonic convulsions. Metoprolol and pindolol antagonized tonic-clonic seizures in DBA/2 mice. Timolol reversed the epileptiform activity of pentylenetetrazol (PTZ) in the brain. Furthermore, amiodarone, the representative of class III AADs, inhibited PTZ- and caffeine-induced convulsions in mice. In the group of class IV AADs, verapamil protected mice against PTZ-induced seizures and inhibited epileptogenesis in amygdala-kindled rats. Verapamil and diltiazem showed moderate anticonvulsant activity in genetically epilepsy prone rats. Additionally, numerous AADs potentiated the anticonvulsant action of AEDs in both experimental and clinical conditions. It should be mentioned, however, that many AADs showed proconvulsant effects in overdose. Moreover, intravenous esmolol and intra-arterial verapamil induced seizures even at therapeutic dose ranges.     

Neuronal plasticity: implications in epilepsy progression and management

Epilepsy is a common neurological disease. A growing number of research studies provide evidence regarding the progressive neuronal damage induced by prolonged seizures or status epilepticus (SE), as well as recurrent brief seizures. Importantly, seizure is only one aspect of epilepsy. However, cognitive and behavioral deficits induced by progressive seizures or antiepileptic treatment can be detrimental to individual function. The neurobiology of epilepsy is poorly understood involving complex cellular and molecular mechanisms. The brain undergoes changes in its basic structure and function, e.g., neural plasticity with an increased susceptibility in neuronal synchronization and network circuit alterations. Some of these changes are transient, while others are permanent with an involvement of both glutamatergic and γ‐aminobutyric acid (GABA)ergic systems. Recent data suggest that impaired neuronal plasticity may underlie the cognitive impairment and behavioral changes associated with epilepsy. Many neurologists recognize that the prevention or suppression of seizures by the use of antiepileptic drugs (AEDs) alone is insufficient without clear predictions of disease outcome. Hence, it is important to understand the molecular mechanisms underlying epileptogenesis because this may allow the development of innovative strategies to prevent or cure this condition. In addition, this realization would have significant impact in reducing the long‐term adverse consequences of the disease, including neurocognitive and behavioral adverse effects. Drug Dev Res 68:498–511, 2007. © 2008 Wiley‐Liss, Inc.